Sacral fractures have not been described well in dogs. The records of 32 dogs diagnosed with sacral fractures were evaluated for neurologic deficits at presentation and discharge. Follow-up was in the form of telephone survey or physical examination at recheck. A score was assigned for each dog at presentation, discharge, and follow-up (0 for normal, 1 for minor deficits, and 2 for major deficits). Fractures located lateral to the sacral foramina were called abaxial, and those medial to the sacral foramina were called axial. Axial fractures had significantly more severe deficits at presentation (p = 0.00017) and discharge (p = 0.03063), but not at follow-up. Neurologic status did not improve significantly during hospitalization in either fracture group, but had improved significantly at follow-up.
Lymphosarcoma of the cauda equina in a domestic shorthair cat invaded the body of L7 and cranial portion of the sacrum. Clinical signs consisted of acute ambulatory paraparesis, tail paralysis, and dyschezia. Radiographically, there was evidence of bone lysis. Surgical exploration yielded a diagnosis, but did not induce improvement in the cat, which was subsequently euthanatized. Neurologic signs were similar to those associated with sacral nerve root avulsion injuries in cats.
Neospora caninum, a protozoan organism, caused extensor rigidity of the pelvic limbs in a 12-week-old dog. Diagnosis was based on results of muscle biopsy, neuroelectrodiagnostics, serotesting, and cell culture. Indirect fluorescent antibody (IFA) titer to N caninum was 1:800 at time of admission and 1:3,200 after 4 and 6 weeks. A reciprocal IFA titer of 50 to N caninum was also found in the CSF. Serotesting for T gondii was negative. Treatment with clindamycin followed by sulfadiazine and trimethoprim did not change the pelvic limb extensor rigidity, but other signs of minor neurologic dysfunction improved.
Abstract Objective To study biomechanical characteristics of the normal and surgically altered canine thoracolumbar vertebral column to determine the effects of surgery and trauma on lateral stability. Animals The T13-L1 vertebral motion units of 48 mixed-breed dogs were dissected free of surrounding musculature and prepared for biomechanical testing by cross-pinning the vertebral bodies and mounting in polymethylmethacrylate. Procedure Normal and surgically altered spinal specimens were subjected to lateral bending. The mean slope of the bending moment versus angular displacement curve and the load to failure were compared between treatment groups and significance was determined by the method of least squares ( P < 0.05). Specimens were surgically altered by facetectomy, lateral fenestration, diskectomy, and combinations of these procedures. Each specimen was subjected to lateral bending to failure at a rate of 2.5 cm/min in a swing arm bending jig designed to simulate 4-point bending and subject the specimen to pure bending. Results Only specimens undergoing diskectomy had a significant decrease in slope and load at failure. Unilateral and bilateral facetectomies and fenestration induced a nonsignificant decrease in stiffness, compared with control specimens. Conclusions Fenestrations and facetectomies do not appear to increase the risk of injury to the canine thoracolumbar spinal cord during lateral bending. Clinical Relevance Fenestrations and facetectomies, as used in routine laminectomies, may be performed without concern for significant destabilization of the spine in lateral bending; however, it is possible that thoracolumbar spinal fractures involving only the vertebral body may significantly destabilize the spine in all modes of bending. ( Am J Vet Res 1996;57:1228-1232)
The adult chicken provides the generally accepted animal model for organophosphorus‐induced delayed neuropathy, exhibiting both clinical signs and histopathological damage after exposure. In this study, noninvasive electrodiagnostic methods were used for assessment of the development of neuropathy after administration of a single dose of protoxicant tri‐ortbo‐tolyl phosphate (TOTP, 360 and 500 mg/kg po) and active congener phenyl saligen phosphate (PSP, 2.5 and 6 mg/kg im). Onset and severity of clinical signs were dose‐related for both organophosphorus compounds. Extensive peripheral nerve lesions consistent with advanced stages of organophosphorus‐induced delayed neuropathy were noted in selected chickens examined 19 d after TOTP administration. Needle electromyographic examinations of gastrocnemius, anterior tibialis, semitendinosus, and semimembranosus muscles were done before exposure and on d 8, 15, and 19 after exposure to TOTP and on d 8, 15 and 17 after exposure to PSP. Untreated chickens (negative controls) were also examined at each session. An untreated chicken with a transected sciatic nerve (positive control) was examined on d 13, 20, and 23 posttransection. Prolonged insertional activities were found in both treated and untreated chickens. Denervation potentials were found in only 2 of the 20 chickens administered organophosphates. Denervation potentials were, however, easily visible 13 d following transection of the sciatic nerve of a normal chicken. Needle electromyography could not evaluate organophosphorus‐induced delayed neuropathy in chickens of this study.
Peripheral hypomyelinization was found in 2 Golden Retriever littermates that had pelvic limb ataxia, depressed postural reactions, and depressed segmental reflexes. Diagnostic findings included infrequent denervation potentials, reduced or absent evoked potentials, and markedly diminished motor nerve conduction velocities. Light and electron microscopy of peripheral nerves revealed fewer than normal myelinated axons, myelinated sheaths inappropriately thin for the caliber of the fiber, poor myelin compaction, greater than normal numbers of Schwann cell nuclei, many Schwann cells with voluminous cytoplasm, and greater than normal amount of perineural collagen. Findings were compatible with a peripheral hypomyelinization process; a defect in Schwann cell function was suspected.
Objective. To establish signalment and phenomenology of canine idiopathic head tremor syndrome (IHTS), an episodic head movement disorder of undetermined pathogenesis. Design. Retrospective case series. Animals. 291 dogs with IHTS diagnosed between 1999 and 2013. Procedures. Clinical information was obtained from an online community of veterinary information aggregation and exchange (Veterinary Information Network, 777 W Covell Boulevard, Davis, CA 95616) and conducted with their approval. Information on breed, sex, age of onset, tremor description, mentation during the event, effect of distractions and drugs, diagnostics, presence of other problems, and outcome was analyzed. Results. IHTS was found in 24 pure breeds. Bulldogs, Labrador Retrievers, Boxers, and Doberman Pinschers comprised 69%; mixed breeds comprised 17%. Average onset age was 29 months (range: 3 months to 12 years). First episode occurred before 48 months of age in 88%. Vertical (35%), horizontal (50%), and rotational (15%) movements were documented. Possible trigger events were found in 21%. Mentation was normal in 93%. Distractions abated the tremor in 87%. Most dogs did not respond to antiepileptic drugs. Conclusions and Clinical Relevance. This retrospective study documents IHTS in many breeds including Labrador Retrievers, Boxers, and mixed breeds.
